JC26 (Medicine) - Headache and Neuralgia Flashcards
Differentiate primary and secondary headache
□ Primary headache (~90%): benign headaches that does NOT arise from structural brain lesions
□ Secondary headache: headache occurs as a symptom of an underlying disease
5 most common types of headaches
Tension type headache (50-70%)
Migraine (10-15%)
Medication overuse
Cluster headache
Raised ICP
Pathophysiology of headache (pain sensitive structures)
Headache results from pressure, traction, displacement or inflammation of nociceptors in head
Intracranial pain-sensitive structures:
□ Vessels: venous sinuses, cortical veins, basal arteries
□ Dura
Extracranial pain-sensitive structures:
□ Scalp: vessels and muscles
□ Orbit
□ Cavities: oral, nasal, paranasal sinuses
□ Ear: external and middle ear
List 4 primary headaches
Tension-type headaches
Migraine
Cluster headache
Headache associated with specific activities
List secondary causes of headaches
Raised ICP
Meningitis
Temporal arteritis
Subarachnoid hemorrhage
Cervical spondylosis
Others:
- Vascular: carotid/vertebral dissection, hypertensive crisis, vasculitis
- CSF: CSF hypotension, post-LP headache
- Other cranial structures: acute glaucoma, head trauma, neuralgia (post-herpetic, trigeminal, occipital)
Features of Tension-type headache
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Bilateral, generalized, radiate forwards from occipital region
- Band-like tightness lasting for hours to weeks, recur often
- No associated symptoms, pt can carry on with activities
Time course: last for hours to days or even months → May be episodic or chronic (persist over years)
- Wax and wane, worse on touching scalp and worse in later part of day
- Can be associated with anxiety/depression/ stress
Tension-type headache
- Pathophysiology
- Treatment
Pathophysiology: incompletely understood
□ A/w stress, anxiety and underlying depression
□ Muscular in origin: likely a misinterpretation of sensory afferents from epicranial muscles as pain
Treatment:
Short-term (abortive): NSAIDs, COX-2 inhibitor, paracetamol, combination
Long-term (prophylactic):
→ Pharmacological: amitriptylline
→ Nonpharmacological: behavioural therapy
Features of migraine
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Unilateral severe and Pulsatile/ Throbbing pain for 4-72h
- 20% preceded by aura (99% visual, 31% sensory, 18% aphasic, 6% motor)
- Associated with photophobia, phonophobia, nausea/vomiting
- Debilitating (worsens by movement) → lies in a quiet, dark room
Features of Cluster headache
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Severe, unilateral periorbital pain for 15-180 min
- Strikingly periodic – begin at same hour for consecutive days over weeks
- Associated with autonomic features eg. unilateral lacrimation, nasal congestion, conjunctival injection, Horner’s syndrome (~30-50%)
- highly agitated during attacks
Features of Headache due to Raised ICP
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Generalized headache, worse in morning
- Associated with drowsiness, LOC or nausea/vomiting
- Often worsen with coughing and sneezing and relieved with vomiting
Features of Headache due to Meningitis
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Generalized headache with neck stiffness of gradual onset/ meningism
- Associated with photophobia, ↓consciousness and fever
Features of Headache due to Temporal arteritis
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Persistent unil/bil temporal headache in pt >50y/o
- Associated with temporal tenderness, jaw claudication, diplopia or amaurosis fugax
Jaw claudication - pain in proximal jaw near TMJ after brief chewing of tough food
Features of Headache due to SAH
Location, character, associated symptoms, temporal course, relieving/ exacerbating factor
- Thunderclap (worst) headache with often dramatic onset
- Initially localized (often occipital) but becomes generalized
- Commonly occurs on physical exertion, straining and sexual excitement
- Associated with meningism (late, after 6h) ± LOC
Features of Headache due to Cervical spondylosis
Location, character, associated symptoms
- Commonly over occipital region (supplied by upper cervical roots)
- Can be a/w neck stiffness (less limited to flexion/extension) or pain
7 questions to characterize headache
Characterize the headache:
1) New onset or chronic?
2) Prodrome/precipitation
3) Quality
4) Region
5) Severity
6) Temporal course: acute vs subacute vs chronic
7) Associating symptoms
Ddx types of headache with bilateral vs unilateral involvement, ocular or facial involvment
→ Bilateral (TTH, ↑ICP, …) vs unilateral (migraine, cluster, temporal arteritis, trigeminal)
→ Ocular: ocular diseases (eg. acute glaucoma), trigeminal autonomic cephalalgias (TACs), lesions at apex of orbit or cavernous sinus (rare)
→ Facial: trigeminal neuralgia, herpes zoster, post-herpetic neuralgia, dental/TMJ diseases, sinusitis
Red flag signs of severe secondary causes of headache (5)
- Systemic upset (constitutional symptoms): CNS infection, Neoplasia, Vasculitis
- Neurological S/S: Intracranial pathologies
- New, Sudden onset: Temporal arteritis, SAH, Anneurysms, Dissections, Hypertensive crises, Acute optic neuritis, acute glaucoma, hydrocephalus
- Associated symptoms: trauma (haematoma), vomiting (ICP), Rash (meningococcus), Visual (glaucoma)
- Progression or Persistent despite treatment
Primary headaches
- Compare onset and duration between Migraine, Tension and Cluster headache
Migraine: Gradual onset, crescendo; 4-72 hours
Tension: Gradual onset, wax-and-wane; 30min – 7d
Cluster: Rapid onset; 15min – 3h
Primary headaches
Compare triggers, quality and associated symptoms
Migraine:
- Trigger: Premenstrual, stress, exercise
- Quality: Unilateral pulsating, moderate to severe, Debilitating (worsen by movement)
- Nausea/vomiting, Photophobia, phonophobia, Preceded by aura
Tension:
- Trigger: emotions, stress
- Bilateral band-like tightness
- No associated symptoms
Cluster
- Trigger: Alcohol, HTN
- Severe unilateral periorbital pain, deep and piercing, restless
- Ipsilateral autonomic features ((lacrimation, nasal congestion, conjunctival injection, Horner’s)
First line investigations for headache
P/E: Full neurological exam + H&N exam (skull, C-spine, teeth, ENT, sinuses, eyes) + BP
Investigations: for suspected serious secondary cause:
- CBC, L/RFT for systemic disease
- ESR
- Plain XR e.g. CXR
- CT/MRI brain (neurological deficits or seizures)
- Vascular imaging
- LP CSF analysis (infective or infiltrative)
- ENT evaluation
Management of migraine
Triggers, abortive Tx and Prophylatic Tx
Management of Tension type headache
Triggers, abortive Tx and Prophylatic Tx
Management of Cluster headache
Triggers, abortive Tx and Prophylatic Tx
Causes of acute headache (9)
- SAH
- Primary heachache: Migraine, Cluster headache
- Glaucoma
- Arterial dissection: carotid, vertebral
- Retrobulbar neuritis
- Trauma
- Drugs/ toxins
- Hydrocephalus
- Infection: meningitis/ encephalitis, sinusitis
Causes of subacute headache (7)
- Infection: e.g. chronic meningitis, TB, brain abscess
- Intracranial tumor
- Chronic subdural haematoma
- Hydrocephalus
- Idiopathic intracranial hypertension
- Temporal arteritis
- Intracranial hypotension
Causes of chronic headache (6)
- Tension-type headache
- Transformed migraine
- Medication overuse headache
- Ocular eye strain/ Refractive error
- Drugs/ toxins (e.g. vasodilators)
- Cervical spondylosis
Migraine
- Frequency for clinical Dx
- Clinical subtypes
Definition: migraine patient defined as
□ ≥2 attacks with aura
□ ≥5 attacks without aura
Types:
□ Migraine with aura (20%): with a warning of visual, sensory or motor type followed by headache
□ Migraine without aura (80%): without aura symptoms
□ Mixed: Up to 33%
Migraine pathophysiology
Pathophysiology: still unclear
□ Cortical spreading depression (CSD): dysfunctional ion channels → spreading front of cortical depolarization followed by hyperpolarization → ‘aura’ symptoms
□ Neurogenic inflammation: CSD → stimulation of trigeminal nerve endings at cranial vessels → nociceptive neurones on dural blood vessels release plasma proteins and pain neurotransmitters → ‘neurogenic inflammation’ with vasodilatation
□ Pain due to activation of nociceptors and central pain sensitization (∵dysfunction of BS pathways that normally modulate sensory input, eg. dorsal raphe nucleus, locus ceruleus…)
Migraine
Temporal Phases and associated features
Typical course of migraine:
□ Prodrome (77%): preceding mental and mood fluctuations, fatigue or autonomic symptoms for 24-48h
□ Aura: gradual development of transient focal neurological symptoms; develop over 4-60min before/ during headache
□ Headache: moderate-severe unilateral or bilateral pulsating headache for 4-72h
□ Postdrome: hangover-like state w/ listlessness + sudden head mov’t trigger headache for up to 24h
Describe different types of migraine aura
Visual (99%):
- Scotoma (-ve): gradually spreading visual defect, often bordered by fortification spectra
- Fortification spectra (+ve): shimmering, silvery zig-zag lines that march across visual fields
Sensory: (31%): tingling (+ve) followed by numbness (-ve) spreading from one part of the body to another
Aphasic (18%): transient speech disturbance due to dominant hemisphere involvement
Motor (6%): hemiplegic aura
Complications of migraines
- Chronic migraine if ≥15d/mo for >3mo w/o medication overuse
- Status migrainosus: debilitating migraine attack lasting for >72h
- Persistent aura w/o infarction: if aura lasts for >1w
- Migrainous infarction: aura symptoms lasting for >1h + ischaemic infarct on CT/MRI
- Migraine-triggered seizure: epileptic seizure occur during or ≤1h of aura
Describe one hereditary primary headache
Familial hemiplegic migraine (FHM):
□ Cause: mutations in VGCC α1 subunits (FHM1) or Na+/K+/ATPase α2 subunit (FHM2)
□ Pathophysiology: changes in ion transport → hyper neuronal excitability → susceptibility to cortical spreading depression
Triggers of migraine
→ Dietary: alcohol, chocolate, tyramine-containing (eg. dairy products), starvation, caffeine
→ Hormonal: often premenstrual or related to OCP (fluctuation in oestrogen)
→ Emotional: stress, anger, excitement
→ Others: change in sleep, irregular meals, certain drugs, smoking, fluorescent lights,
weather
Management of acute migraine attack
simple analgesics for mild attacks, migraine-specific agents for severe attacks
Simple analgesics: aspirin, paracetamol, NSAIDs, combination
D2-blocker anti-emetic (↓nausea/vomiting + ↓headache): metoclopramide, domperidone
Triptans for severe headache: sumatriptan (oral, subcutaneous, nasal), naratriptan (PO), zolmitriptan (PO)
Ergotamine (also 5HT1 agonist like Triptan)
Triptans
- Indication
- MoA
- S/E
- C/I
- Indication: Severe migraine headache
- MoA: 5HT1 agonist → vasoconstriction, peripheral neuronal inhibition, ↓trigeminal neurotransmission
- S/E: dizziness, somnolence, asthenia, nausea
- C/I: IHD, stroke, CAD, uncontrolled HTN
Ergotamine
- Indication
- MoA
- S/E
- C/I
- Indication: Severe migraine headache
- MoA: 5HT1 agonist → vasoconstriction, ↓trigeminal neurotransmission
- S/E: vascular events (sustained generalized vasoconstriction), high risk of overuse syndrome and rebound headache
- C/I: IHD, thyrotoxic heart disease, PVD, uncontrolled HTN
Prophylactic drugs for recurrent migraine
- Indication
- Drug types
- Indication
- Attacks weekly or >2 times a month
- Attacks less often but very prolonged and debilitating
- Drug types
- Prophylactic NSAIDs in menstrual or orgasmic migraine
- Antihypertensives: β-blockers, CCB
- Antidepressants: amitriptyline, venlafaxine
- Anticonvulsants: topiramate, valproate
- CGRP antagonists, eg. erenumab, fremanezumab, galceanezumab
- Others: pizotifen (5HT2 blocker), botox injections around H&N q12w (if refractory)
Precautions of using analgesics for migraine attacks
- Limit to 2-3d/week → Limit medication overuse headache
- Keep headache diary → monitor for escalation in drug use
- Avoid opioids: mask pain without suppressing pathophysiological mechanism → cognitive impairment or addiction
Medication overuse headache
- Character
- Cause
- Mx
Character:
→ Gradual ↑headache frequency and drug consumption
→ Change in headache characteristics
→ Ultimately take analgesics and large amounts of caffeine
Causes
daily analgesic use (>10-15d/month) or compound analgesics (esp opiates) and triptans
Mx
Abrupt withdrawal from painkillers or antimigraine drugs
Define Trigeminal autonomic cephalalgias (TACs)
3 examples
syndromes with combination of facial pain and autonomic dysfunction
□ Cluster headache: severe unilateral periorbital pain of 10min-3h + unilateral autonomic activation
□ Paroxysmal hemicrania: similar to cluster headaches but shorter (2-45min)
□ SUNCT: brief, severe, sharp periorbital pain (15s-3min) a/w conjunctival injection and tearing, ↑by touch or neck movement
Cluster headache
- Pathophysiology
- Clinical types
- S/S
Pathophysiology: unknown, a/w
Abnormal hypothalamic or thalamic activity
Paroxysmal discharges of central trigeminal and PN pathways
Types:
Episodic: clusters (7-365d) with pain-free remissions (>1mo)
Chronic: recurrent attacks (>1y) without or with pain-free remissions <1mo
S/S:
Headache: extreme unilateral periorbital piercing/throbbing pain
Autonomic features: unilateral lacrimation, nasal congestion, conjunctival injection, sweating ± transient Horner’s syndrome
Agitation
Periodic pain daily with clustering period of pain over days, followed by pain-free periods
Management of cluster headache (acute attack and prophylaxis)
Acute attacks:
→ SC sumatriptan OR 100% O2 (15L/min) as 1st line
→ Intranasal lidocaine (administered ipsilaterally)
→ PO ergotamine or IV dihydroergotamine (5HT1 agonist)
Prophylaxis: should be started during cluster periods
→ Verapamil
→ Short course oral corticosteroids
→ Other drugs: topiramate, methysergide, gabapentin, Lithium
Secondary causes of cluster headache
intracranial large artery aneurysms, AVMs, cavernous haemangiomas, meningiomas…
Giant cell arteritis
- Pathophysiology
Pathology: subacute granulomatous inflammation of large/medium sized arteries with lymphocyte, plasma cell, neutrophil and giant cell infiltration
□ Results:
→ Thrombosis due to vessel wall thickening:
- Ophthalmic artery → amaurosis fugax
- Basilar artery → posterior circulation infarct
→ Stimulation of nociceptive neurones → pain
□ Site: often involves superficial temporal artery → tender, thickened, non-pulsatile on examination
S/S of Giant cell arteritis
□ Headache: new onset, bitemporal, intense throbbing headache
□ Neurological S/S:
Stroke, hearing loss, myelopathy, neuropathy
Blindness due to acute ischaemic optic neuropathy (AION)
□ Jaw claudication: pain when chewing or talking due to ischaemia of masseter
□ Visual S/S: amaurosis fugax (transient), can progress into permanent blindness (sight-threatening)
Due to arteritic acute ischaemic optic neuropathy (AAION)
□ Systemic S/S:
Fever, anorexia, malaise
Polymyalgia rheumatica (50%): pain and stiffness over shoulder and pelvic girdle muscles
Diagnostic criteria for Giant cell arteritis
Diagnostic criteria: ≥3 criteria
(1) Onset ≥50y
(2) New headache
(3) Abnormalities of temporal artery at PE: tender, thickened, non-pulsatile superficial temporal artery
(4) ↑ESR (>50mm/h)
(5) Abnormal findings on biopsy of temporal artery
Treatment of Giant Cell Arteritis
Tx: urgent prednisolone 60mg qd
□ Urgent Tx prevents blindness and brainstem stroke and ↓headache
□ Parenteral high dose if complications already occurred
□ Gradual ↓dosage to maintenance level according to ESR level
Neuralgia
- Features of pain
- Temporal course
- Trigger
□ Sudden intense sharp, aching, lancinating, burning, stabbing pain in distribution of nerve
□ Lasts seconds to <2min, occurring repeatedly within short periods
□ Often triggered by sensory/mechanical stimulus
Name most frequent neuralgia
S/S
Triggers
Temporal course
Trigeminal Neuralgia
S/S: paroxysmal attacks of unilateral severe, short, sharp, stabbing pain
Site: typically unilaterally following V2 or V3 distribution
Triggers: spontaneous or touching a specific spot or doing certain activities (eg. touching/washing face, shaving, brushing teeth, chewing)
Course:
→ Paroxysmal attacks for many times per day, lasting several days or weeks
→ Then stop abruptly followed by pain-free periods for months or years
→ Tend to become more frequent over years with ↓duration of remission periods
Causes of trigeminal neuralgia
□ Classical TN:
→ Vascular loop compression: most common, 80-90%
→ Idiopathic
□ Other causes (secondary TN):
→ Multiple sclerosis, esp young and when bilateral
→ CPA masses: vestibular neuroma, meningioma, epidermoid cyst, AVM, angiomas…
→ Herpes zoster and post-herpetic neuralgia
Treatment of Trigeminal neuralgia
Medical Tx: for classic TN
Carbamazepine (first-line, most effective, 75% responsive)
Surgical Tx: for refractory classic TN
- Peripheral neurectomy, eg. alcohol ablation (temporary relief)
- Microvascular decompression (separate vessels from trigeminal nerve root)
- Percutaneous radiofrequency thermocoagulation rhizotomy (artificial lesion for trigger spot on Trigeminal nerve)
Treatment of underlying condition (eg. surgical decompression) for secondary TN
